Neuroinflammation and Alzheimer’s disease: the role of microglia in brain homeostasis

Hugh Perry is a consultant at the Dementia Research Institute at University College London (UK) and leads the Neuroinflammation Theme across the Dementia Research Institute Centers. His job is to encourage and foster collaboration in neuroinflammation across the Institutes and to use its intellectual capital and fantastic resources to gain insights into neurodegeneration disease process. Previously, Hugh trained as a neuroscientist at the University of Oxford (UK), he then moved to the University of Southampton (UK) to continue to lead a laboratory in neuroinflammation.

In this interview, Hugh speaks to us about a big topic in dementia research right now, which is the role of neuroinflammation in Alzheimer’s disease. He provides us with a brief overview of neuroinflammation in Alzheimer’s disease and explains why it might be a good idea to push microglia back to their homeostatic levels, as opposed to pushing them towards phagocytosis.

1.What is your current research focus and what inspired you to work in this area?

For the last 25 years, my research focus has been centered on the role of microglia in neurodegenerative diseases, including inflammatory diseases such as multiple sclerosis, and their role in communicating systemic inflammation to the brain. My laboratory is probably well known for its work on microglia biology.

2.You presented a talk at the Alzheimer’s Research UK Conference (19–20 March, Harrogate, UK) on neuroinflammation and Alzheimer’s disease – could you provide us with a brief overview about this?

“Thus, this has turned the attention from microglia activation being simply a consequence of the disease to microglia contributing to the disease process.”

For many years, people have discussed what the role of microglia in Alzheimer’s disease might be. Like many other neurodegenerative diseases, Alzheimer’s neuropathology is associated with an increase in the numbers of microglia, and a phenotypic change typically referred to as microglia activation.

The big issue for many years was whether this microglia activation was simply a consequence of ongoing pathology, a response to the degeneration of neurons, and thus activation of these innate immune cells, or whether they were actually contributing to the disease.

In the last 10 years, this landscape has changed dramatically and this is because of GWAS studies. What these GWAS and other genetic studies have shown us is that there are a large number of genes with small effects that impact the risk of Alzheimer’s disease, and perhaps surprisingly a significant proportion of these turn out to be genes that are expressed by cells of the myeloid lineage.

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